KEY QUESTIONS IN SURGICAL CRITICAL CARE - PART 8 ppsx

Key Questions in Surgical Critical Care 161 Vivas Cardiovascular System Answers Cardiac output Measurement of cardiac output is useful both as a diagnostic aid and to monitor therapy in the critically ill patient. A low cardiac output in the hypotensive patient is consistent with cardiogenic shock and indicates the need for inotropic support, while a high cardiac output is consistent with septic shock. SVR In the clinical setting, the determination of SVR is often used together with cardiac output and PAOP to assist in the diagnosis of the shocked patient (Table 1.3). A low SVR is characteristic of septic shock, while the SVR is usually raised in cardiogenic shock and hypovolaemia. Serial measurements of PAOP, cardiac output and SVR can be used to monitor the effects of fluid administration and inotropic therapy. Blood oxygen saturations The differential diagnosis of the patient in cardiogenic shock after acute myocardial infarction includes VSD and mitral regurgitation due to papillary muscle rupture. Differentiating between the two may be difficult because both cause similar clinical presentations and a pansystolic murmur. If the diagnosis cannot be made by echo, then blood oxygen saturations can be measured from the right ventricle and right atrium. A ‘step-up’ in oxygen saturation in the right ventricle (oxygen saturation higher than the right atrium) would be consistent with a VSD. Mixed venous (pulmonary artery) blood oxygen saturation measurement is required for estimation of cardiac output by the Fick method. Table 1.3 The differential diagnosis of shock using haemodynamic parameters obtained from Swan-Ganz catheterisation PAOP Cardiac index SVR Hypovolaemia ↓↓↑ Cardiogenic shock ↑↓↑ Septic shock ↓↑↓ PAOP ϭ pulmonary artery occlusion pressure; SVR ϭ systemic vascular resistance; Normal values: PCWP 8–12 mmHg; Cardiac index 2.5–4.0 l/min/m 2 ; SVR 770–1500 dynes s/cm 5 pp 18–20 SCC Kqs-A-s2-1.qxd 5/11/02 11:26 AM Page 161 Key Questions in Surgical Critical Care 162 Vivas Cardiovascular System Answers 9. What are the complications of blood transfusion? 9. The possible complications of blood transfusion are: precipitation of heart failure, febrile reaction, haemolytic transfusion reaction, transmission of infection, hyperkalaemia, hypocalcaemia, thrombocytopenia, disseminated intravascular coagulation (DIC), hypothermia. Haemolytic transfusion reactions are usually due to ABO incompatibility caused by administrative error. They should be managed by stopping the blood transfusion, checking patient identity against the blood unit, returning the blood unit to the haematology laboratory with a sample of clotted blood and ethylene diamintetraacetic acid (EDTA) sample. Severe reactions may require the administration of fluid, adrenaline, antihistamine and steroids as for anaphylactic shock. Milder febrile reactions are usually due to antibodies against white cells. A number of infections (viruses, bacteria, protozoa) can be transmitted by blood transfusions. Most concern surrounds the transmission of viral infections including hepatitis B & C, human immunodeficiency virus (HIV), Epstein-Barr virus (EBV), and cytomegalo virus (CMV). Antibodies against hepatitis B & C, and HIV are screened for in blood donated in the UK. Massive transfusion (defined as a transfusion volume equal to the patient’s own blood volume within 24 hours) may be associated with several complications. Stored blood contains few platelets and reduced concentrations of factors V and VIII. ‘Dilutional’ thrombocytopenia and clotting factor deficiency may therefore occur during massive transfusion. The platelet count, INR and activated partial thromboplastin time (APTT) should be monitored, and the administration of platelets and fresh frozen plasma may be required. The plasma potassium concentration increases during storage as potassium leaks out of the red cells. Plasma calcium levels may be reduced by binding of ionised calcium by citrate added to stored blood. Hypocalcaemia and hyperkalaemia may therefore occasionally result after massive transfusion. Hypothermia may result from the rapid transfusion of blood and blood warmers should be used during rapid massive transfusion. pp 38–41 SCC A Q Kqs-A-s2-1.qxd 5/11/02 11:26 AM Page 162 Key Questions in Surgical Critical Care 163 Vivas Cardiovascular System Answers 10. How would you manage the acute onset of atrial fibrillation (AF)? 10. AF is characterised by the absence of a P wave before each QRS complex and irregularity of the ventricular (QRS) response (Fig. 1.2). Management includes the identification and correction of reversible causes such as electrolyte imbalance. Further management depends upon whether haemodynamic compromise is present and on the ventricular rate. If significant haemodynamic compromise is thought to be caused by the new occurrence of AF, then DC cardioversion should be performed urgently. If the patient is not significantly compromised, then he can either be managed with ventricular rate control or by elective cardioversion. Digoxin, ␤-blockers and verapamil can be used for rate control. Cardioversion may be attempted chemically or electrically. A number of anti-arrhythmic drugs can be used to cardiovert AF to sinus rhythm, but success is limited and they all carry the risk of pro-arrhythmia, particularly if the heart is not structurally normal. Amiodarone and ␤-blockers are the safest drugs in the structurally abnormal heart. DC cardioversion carries a higher success rate. Cardioversion can be performed without anticoagulation if the onset of AF occurred within 48 hours, as A Q Fig. 1.2 Electrocardiogram (ECG) demonstrating atrial fibrillation. aVRI II III II aVL V1 V2 V4 V5 aVF V3 V6 Kqs-A-s2-1.qxd 5/11/02 11:26 AM Page 163 Key Questions in Surgical Critical Care 164 Vivas Cardiovascular System Answers the risk of left atrial thrombus formation is low within this time frame. Thereafter, 4 weeks of warfarin prior to cardioversion (as an outpatient) is recommended. All patients with persistent AF, except those aged Ͻ65 years with lone AF, should be considered for warfarin to prevent stroke. pp 20–21 11. How would you treat acute pulmonary oedema? 11. Reassure the patient. Sit him up. Monitor ECG and oxygen saturations. Administer high flow oxygen via a rebreathing bag. Give intravenous opiate (e.g. diamorpine 2.5–5 mg) and anti-emetic (e.g. metaclopramide 10 mg). Opiates act as venodilators, reducing preload, and also as an anxiolytic. Administer intravenous diuretic (e.g. frusemide 40 mg). Acutely, this acts as a venodilator prior to the onset of its diuretic effect. If the patient is not hypotensive, initiate an intravenous nitrate infusion. Again, this causes vasodilatation and reduces preload. As pulmonary venous pressure falls to the threshold at which plasma oncotic pressure favours resorption of fluid, pulmonary oedema begins to resolve. If the patient is hypotensive (cardiogenic shock), inotropes (e.g. dobutamine 2.5–15 ␮g/kg/min) should be initiated. The dose is tailored to achieve a blood pressure capable of perfusing the major organs. Clinically, this is reflected by a satisfactory urine output. pp 33–35 12. How would you manage the acutely unwell patient with sudden onset chest pain radiating to the back and an absent right brachial and radial pulse? 12. The likely diagnosis is aortic dissection, but myocardial ischaemia with right subclavian artery stenosis due to atherosclerosis, and emboli to the brachial artery and a coronary artery due to left atrial thrombus or endocarditis, are possible. Monitoring of vital signs, ECG and oxygen saturations should be performed. Oxygen and opiate analgesia should be administered. Examination of the patient should focus on determining the contralateral BP, the presence or absence of the other peripheral pulses and of aortic regurgitation. A Q SCC A Q SCC Kqs-A-s2-1.qxd 5/11/02 11:26 AM Page 164 Key Questions in Surgical Critical Care 165 Vivas Cardiovascular System Answers Blood tests will include full blood count (FBC), U & E, and cross-match. Initial investigations may provide supportive evidence for the diagnosis of aortic dissection. A 12-lead ECG should be performed. However, any of these scenarios may produce ST segment changes of ischaemia or infarction. In aortic dissection, this is caused if a coronary artery ostium is disrupted by the dissection flap. Transthoracic echo may demonstrate the dissection flap, and will also demonstrate the presence of aortic regurgitation and pericardial effusion, both consistent with aortic dissection. CXR may reveal a widened mediastinum and/or a pericardial effusion in cases of aortic dissection. The definitive diagnosis is usually made by either contrast- enhanced CT scan, magnetic resonance imaging (MRI) or transoesophageal echo (TOE). This depends largely on local availability and expertise. CT scanning is readily available and non-invasive. MRI tends to be less readily available and it presents difficulties in monitoring of the acutely ill patient. TOE requires an experienced operator, but can be performed on the ward or in the anaesthetic room and provides additional information about the presence of aortic regurgitation, pericardial effusion, left ventricular function and relationship of the coronary ostea to the dissection flap. Aortography is now rarely used because it is invasive and potentially complicated by catheters entering the false lumen. Further management is dependent upon the site of the dissection. Stanford type A dissections involve the ascending aorta and are managed surgically, while type B dissections do not involve the ascending aorta and are managed medically unless complications ensue. The mainstay of medical management is control of blood pressure using agents such as intravenous labetalol and sodium nitroprusside to obtain acute control of BP (target 100–120 mmHg systolic), with the addition of oral agents (e.g. ␤-blockers, calcium blockers, ACE inhibitors) thereafter. If distal dissection is complicated by rupture, aneurysm formation, vital organ or limb ischaemia, continued pain, or retrograde progression into the ascending aorta, then surgery is indicated. pp 26–27 SCC Kqs-A-s2-1.qxd 5/11/02 11:26 AM Page 165 Key Questions in Surgical Critical Care 166 Vivas Cardiovascular System Answers 13. Define disseminated intravascular coagulation (DIC). What are the causes and what haematological results would you expect in DIC? 13. DIC is characterised by activation of the clotting cascades with generation of fibrin, consumption of clotting factors and platelets, and secondary activation of fibrinolysis leading to production of fibrinogen degradation products (FDPs). Clinically, it may be asymptomatic manifest only on blood investigations, or may cause bleeding, or tissue ischaemia due to vessel occlusion by fibrin and platelets. DIC may be caused by Gram-negative, meningococcal and staphylococcal septicaemia, tissue damage after trauma, burns or surgery, malignancy, haemolytic blood transfusion reactions, falciparum malaria, snake bites, and obstetric conditions such as placental abruption and amniotic fluid embolism. The prothrombin time (or INR), APTT, and thrombin time are prolonged. The fibrinogen level and platelet count are low. High levels of FDPs are present. There may be fragmented red cells on the blood film due to red cell damage during passage through fibrin webs in the circulation. pp 47–49 14. What are the indications for an intra-aortic balloon pump (IABP)? 14. The intra-aortic ballon pump (IABP) augments diastolic pressure and reduces afterload resulting in increased coronary and cerebral perfusion and a reduction in myocardial oxygen demand. The main indication for an IABP is supportive therapy prior to a definitive procedure. Most commonly, this is in the haemodynamically compromised patient with a post-myocardial infarct VSD or mitral regurgitation due to papillary muscle rupture, or in a patient with ongoing myocardial ischaemia despite maximal medical therapy as a bridge to coronary angioplasty or coronary artery bypass graft surgery. IABP may also be used post-operatively, usually after cardiac surgery, in patients with left ventricular dysfunction. IABP may also be placed prophylactically in high-risk coronary angioplasty. IABP is A Q SCC A Q Kqs-A-s2-1.qxd 5/11/02 11:26 AM Page 166 Key Questions in Surgical Critical Care 167 Vivas Cardiovascular System Answers contra-indicated in patients with significant aortic regurgitation (which it exacerbates), aortic dissection, aortic aneurysm, and severe peripheral vascular disease. p 8 15. What are the potential complications of central vein cannulation? 15. These are: ᭿ arterial puncture, which may result in haemothorax ᭿ pneumothorax ᭿ infection (localised or systemic) ᭿ endocarditis (with chronic central venous cannulation) ᭿ neurological injury ᭿ air embolism. pp 211–214 16. How would you optimise cardiac output in the hypotensive patient? 16. The specific management of the hypotensive patient is clearly partly dependent upon the cause of the haemodynamic compromise. For example, if the hypotension is secondary to haemorrhage, then volume replacement with blood is the treatment. The commonest cause of cardiogenic shock is acute myocardial infarction, which is managed with aspirin, coronary reperfusion by thrombolysis or angioplasty, and inotropes. In the critically ill patient, hypotension may be multifactorial with hypovolaemia, sepsis and left ventricular dysfunction contributing. Certain principles of supportive management can be outlined. Assess and optimise volume status Clinical assessment of volume status comprises searching for a history of blood or volume loss, examining the patient for signs of hypovolaemia or volume overload, examining fluid balance charts, and reviewing a CXR (Table 1.4). A Q SCC A Q SCC Kqs-A-s2-1.qxd 5/11/02 11:26 AM Page 167 Table 1.4 Clinical assessment of volume status in the hypotensive or oliguric patient Hypovolaemia Volume overload History Poor intake or volume loss, Known heart failure e.g. GI bleed, vomiting or suggestive history Examination Postural hypotension, JVP↑, S3, crepitations, jugular venous pressure oedema (JVP)↓, clear lungs, no oedema Fluid balance Negative Positive CXR No pulmonary oedema Pulmonary oedema S3 ϭ third heart sound. Invasive monitoring If volume status remains uncertain after clinical assessment, CVP and/or Swan-Ganz catheter insertion is indicated. In most circumstances, a right-sided filling pressure (CVP) of 10–12 mmHg and a left-sided filling pressure (PAOP) of 16–18 mmHg indicates an appropriate preload to optimise cardiac output. If the filling pressure is too low, fluid should be administered until the PAOP is optimised. Assess the need for inotropes Inotropes are indicated if hypotension is present in the presence of a high PAOP (i.e. the patient is volume overloaded or in cardiogenic shock), or if hypotension persists after correction of hypovolaemia. Assessment of cardiac output and SVR may assist in the diagnosis of the cause of shock (Table 1.3) and in the choice of the appropriate inotropes. In cardiogenic shock, the cardiac output is low and SVR high. In theory therefore the ideal inotrope in these circumstances would increase cardiac output while decreasing SVR. Dobutamine has these properties, at least at lower doses. At higher doses, vasoconstriction and an increase in SVR can occur. In septic shock, cardiac output is usually high and SVR low. Vasoconstricting inotropes e.g. adrenaline or noradrenaline are appropriate. Key Questions in Surgical Critical Care 168 Vivas Cardiovascular System Answers Kqs-A-s2-1.qxd 5/11/02 11:26 AM Page 168 Assess the need for IABP IABP insertion is particularly indicated as supportive therapy prior to a definitive procedure e.g. in a patient with a post-myocardial infarct VSD or mitral regurgitation due to papillary muscle rupture. Treat associated arrhythmias Arrhythmias, particularly AF, are common in the critically ill patient. If the main cause of haemodynamic compromise is thought to be the new occurrence of AF, then DC cardioversion should be performed urgently. Agents such as amiodarone can be used in an attempt to maintain sinus rhythm. More commonly, AF is one of a number of contributing factors and can be managed by control of the ventricular response rate with drugs such as digoxin. Table 1.5 Summary of the optimisation of cardiac output in the critically ill patient Optimise preload If hypovolaemic, replace fluids If volume overloaded, IV glyceryl trinitrate (GTN) and IV furosemide Optimise afterload Sodium nitroprusside or hydralazine Indications for If remains hypotensive despite adequate filling inotropes pressures: Dobutamine Ϯ dopamine for cardiogenic shock Noradrenaline/adrenaline for septic shock Indications for IABP Acute mitral regurgitation or VSD Treat AF Control ventricular response rate Preserved LV function: ␤-blockers, verapamil, diltiazem Impaired LV function: digoxin, amiodarone pp 15–20 SCC Key Questions in Surgical Critical Care 169 Vivas Cardiovascular System Answers Kqs-A-s2-1.qxd 5/11/02 11:26 AM Page 169 Key Questions in Surgical Critical Care 170 Vivas 1. How would you interpret a chest radiograph in a critically ill surgical patient? 1. A system is necessary to ensure that all the appropriate parts of a chest X-ray are reviewed and nothing is missed. ᭿ Is this the correct patient? ᭿ Are there any potentially life threatening abnormalities (e.g. large pneumothorax) ᭿ Assess external lines and leads — Central line — Endotracheal tube (ETT) — Electrocardiogram (ECG) — Chest drains — Pacemaker ᭿ Assess technical aspects — Left and right correctly labelled — Centering of the film — Lung volumes — Penetration ᭿ The lungs — Pulmonary vascular pattern — Hila — Costophrenic region ᭿ The mediastinum — Trachea central or deviated — Left and right heart borders — Heart size ᭿ The soft tissue and bones — Fractures — Free air under the diaphragm pp 75–76 SCC A Q Respiratory System Answers Kqs-A-s2-2.qxd 5/11/02 11:27 AM Page 170 [...]... the cerebrospinal fluid (CSF), but carbon dioxide (CO2) moves freely, allowing rapid reflection of blood CO2 in the CSF ᭿ ↑ CO2 translates to an exaggerated ↓ pH (since the CSF has little buffering capacity) ᭿ The pH change is detected by the central chemoreceptors and stimulates the respiratory centre to increase minute volume Vivas Key Questions in Surgical Critical Care 171 Kqs-A-s 2-2 .qxd 5/11/02... reaches a critical level, preventing further inspiratory effort Proprioceptors – these co-ordinate muscular activity and ventilation Temperature receptors – are responsible for the increase in respiratory rate with fever SCC pp 60–61 Q 4 A 4 172 What is involved in initiating a breath? Inspiration is an active process, initiated by inspiratory neurones in the respiratory centre, located in the floor... floor of the fourth ventricle in the brainstem To initiate a breath the respiratory centre stimulates the respiratory muscles via the cranial and spinal nerves Vivas Key Questions in Surgical Critical Care Kqs-A-s 2-2 .qxd 5/11/02 11:27 AM Page 173 Answers The lungs and chest wall contain stretch and mechanoreceptors, which signal the inspiratory centre via the vagus nerve to end inspiration The stretch receptors... lower ribs, which further increases intra-thoracic volume ᭿ The dilator muscles of the upper airway contract, maintaining patency during inspiration Expiration is usually a passive process of elastic recoil ᭿ ᭿ This is facilitated by the stored energy of the expanded chest wall following inspiration Inspiratory neurones in the brainstem then start firing in response to afferent input from the stretch... ventilation rises from a resting value of 6 8 l/min to values of upto 100 l/min in trained individuals This increase in capacity is mediated by an increase in both respiratory frequency and tidal volume Peripheral chemoreceptors play little role during this process as arterial pH, PaCO2 and PaO2 remain normal Cardiac output also increases upto 30 l/min Oxygen extraction increases secondary to metabolic... of air remaining in the lung after a maximal expiration, and is the minimum amount of air that can be left in the lung ERV is the maximal volume of air that can be expelled after tidal (Vt) expiration Closing capacity (CC): this is the lung volume where small airways begin to collapse on expiration Normally CC is greater than FRC Vivas Key Questions in Surgical Critical Care 175 Kqs-A-s 2-2 .qxd 5/11/02... that can be inspired above tidal (Vt) inspiration ERV ϭ 0.7–1 l: this is the maximal volume of air that can be expelled after tidal (Vt) expiration VC ϭ 3.1–4 .8 l: this is the maximal volume of air that can be expired following a maximal inspiration i.e Vt ϩ IRV ϩ ERV SCC pp 61–67 Key Questions in Surgical Critical Care Kqs-A-s 2-2 .qxd 5/11/02 11:27 AM Page 177 6.0 Inspiratory reserve volume Inspiratory... measured during gas flow and forms a characteristic loop This is caused by the increased effort needed during inspiration to overcome the elastic forces resisting lung expansion Normal expiration is a passive process driven by the stored energy from inspiration The difference between the curves is termed hysteresis (Fig 2.4) SCC pp 62–64 180 Vivas Key Questions in Surgical Critical Care Kqs-A-s 2-2 .qxd 5/11/02... during mechanical (positive pressure) ventilation where preferential ventilation tends towards the upper (non-dependent) areas of the lung This decreases the Vivas Key Questions in Surgical Critical Care 181 Kqs-A-s 2-2 .qxd 5/11/02 11:27 AM Page 182 dependent lung volume and increases V/Q mismatch, leading to arterial hypoxaemia Respiratory System The lung has a mechanism whereby it can improve matching... bicarbonate corrected to a PCO2 of 5.3 kPa, removing the influence of respiratory effects on pH 182 Vivas Key Questions in Surgical Critical Care Kqs-A-s 2-2 .qxd 5/11/02 11:27 AM Page 183 Actual base excess (ABE) – It is an in vitro measurement of metabolic acidosis (Ϫve) or alkalosis (ϩve) PCO2 is corrected to 5.3 kPa, therefore this represents the non-respiratory components only Temperature has a significant . Normal values: PCWP 8 12 mmHg; Cardiac index 2.5–4.0 l/min/m 2 ; SVR 770–1500 dynes s/cm 5 pp 18 20 SCC Kqs-A-s 2-1 .qxd 5/11/02 11:26 AM Page 161 Key Questions in Surgical Critical Care 162 Vivas Cardiovascular. then surgery is indicated. pp 26–27 SCC Kqs-A-s 2-1 .qxd 5/11/02 11:26 AM Page 165 Key Questions in Surgical Critical Care 166 Vivas Cardiovascular System Answers 13. Define disseminated intravascular. ml/cmH 2 O. = change in volume L Compliance change in pressure kP a A Q SCC Kqs-A-s 2-2 .qxd 5/11/02 11:27 AM Page 179 Key Questions in Surgical Critical Care 180 Vivas Respiratory System Answers Factors decreasing